The hypothesis tested was that amiodarone, a potent cardiotonic agent with unknown mechanism of action, has a dose related effect on protection of hypertrophied myocardium. The working isolated rat heart preparation was used at 37 degrees C. Filling pressures and afterload were maintained constant before and after 30 minutes of global ischemia. One injection of 12 ml of normal saline only or containing 0.125-12 mg of amiodarone was given at the onset of ischemia. The determinants of recovery were heart rate, aortic flow, and coronary blood flows. The results show a narrow band width dose response with approximately 40% recovery at 0.125 and 0.5 mg dosages. Maximal recovery of 70% of aortic flow was found at 0.25 mg does. Higher doses produced decremental values of recovery. This study demonstrates that with single dose use at normothermia, amiodarone may be a useful adjunct for cardioplegic solutions but has a narrow dose-response range. Hypothermic drug treated hearts had significantly (p less than .05) enhanced recovery of function vs. normothermic drug treated hearts but differences between hypothermic control and normothermic controls were not signficant (p less than .10) indicating possible synergy or addition between hypothermic and drug effects. It is concluded that amiodarone ameliorated the deleterious effects of global ischemia in hypertrophied rat hearts at normothermic and moderately hypothermic temperatures.